大鼠胃肠嗜铬细胞5－羟色胺合成和分泌与胃黏膜内分泌和腔分泌心房钠尿肽的关系☆

背景：作者前期研究证实心房钠尿肽和5-羟色胺共同存在于胃肠嗜铬细胞的同一分泌颗粒中，那么心房钠尿肽对5-羟色胺的合成与分泌是促进还是抑制，目前仍处于研究阶段。 目的: 通过模拟胃黏膜内分泌和腔分泌心房钠尿肽来证实对胃肠嗜铬细胞中5-羟色胺合成与分泌的影响。 设计：随机对照动物实验。 单位：承德医学院免疫学实验室。 材料：实验于2004-10/2007-07在省级重点实验室承德医学院免疫学实验室完成。选用40只雄性成年Wistar大鼠，由承德医学院实验动物科提供，实验过程中对动物的处置符合动物伦理学标准。实验用心房钠尿肽、5-羟色胺抗体为美国Santa Cruz Biotechnology公司产品。 方法: 随机将40只大鼠均分至内分泌和外分泌2个平行实验中，各分为对照组10只和实验组10只。通过胃腔直接注射心房钠尿肽（28 μg 14 mg/L）模拟外分泌产生的心房钠尿肽，通过舌下静脉注射心房钠尿肽14 μg,14 mg/L)模拟内分泌产生的心房钠尿肽；并以免疫组织化学，透射电镜的超微结构的测量学的方法和高压液相色谱电化学检测的方法对心房钠尿肽刺激后胃内5-羟色胺免疫反应细胞和内分泌颗粒的数量及血清中的5-羟色胺含量，与注射生理盐水的对照组进行对比。 主要观察指标：模拟胃黏膜内分泌和腔分泌心房钠尿肽对胃内5-羟色胺免疫反应阳性细胞密度、分泌颗粒的数密度及血清中的5-羟色胺的影响。 结果: 模拟心房钠尿肽外分泌和内分泌对大鼠胃内5-羟色胺分泌的影响:与对照组相比，胃内5-羟色胺免疫反应阳性细胞密度及分泌颗粒的数密度显著增多(P < 0.05)，血清中的5-羟色胺含量显著减少(P < 0.05)。 结论:外分泌和内分泌的心房钠尿肽对5-羟色胺的释放均有明显的抑制作用。     

两种高压静电场对大鼠血细胞及血清生物化学指标的影响★

目的：从电-机复合系统的认识高度，研究采用生物电阻抗技术的无创胃动力测量和评价方法，研制专用实验检测系统。 方法：采用生物电阻抗技术从体表进行无创胃动力检测，并与同步胃电相结合，研究食物消化过程中的电－机特性，包括节律、传导、胃排空过程以及其影响因素；运用小波变换分离、提取胃阻抗信号；通过能谱和频谱分析方法，根据主能量和支配频率将信号分类; 设置并计算胃动力参数，包括节律、频率谱、功率谱、动态谱、主频变异系数FIC、主频下功率变异系数PIC等。 结果：建立了生物电阻抗无创胃动力测量和评价方法，研制了专用实验检测系统。28例受试者在不同时段的胃动力对照实验结果表明，胃动力参数2~4 cpm收缩节律比、2~4 cpm功率比、主频变异系数FIC在下午时段比上午明显增加，但主频下功率变异系数PIC没有显著性变化；餐前、餐后胃动力对照实验结果表明，空腹时胃运动的节律比较紊乱，进食后节律性增加；药物对胃动力影响实验表明铝碳酸镁片的作用在于中和胃酸，多潘立酮片有促进胃动力的功效。 结论：采用无创生物阻抗方法和同步胃电测量相结合的技术，可研究复杂的胃动力电－机过程，包括节律性、传导性、胃排空过程以及影响因素，可为胃动力测量和评价提供一种新的、有效的无创方法。     

GM_1对大鼠全脑缺血再灌注中钙平衡紊乱、氧自由基代谢异常以及病理损伤的影响

目的　研究单唾液酸四已糖神经节苷脂（ＧＭ１）对大鼠全脑缺血再灌注中钙平衡紊乱、氧自由基代谢异常以及病理损伤的影响。方法　运用大鼠全脑缺血再灌注模型（４ＶＯ）,观察假手术组、脑缺血３０ 分钟再灌注６０ 分钟生理盐水（ＮＳ）处理组（ＮＳ组）和缺血３０ 分钟再灌注６０ 分钟ＧＭ１ 处理组（ＧＭ１ 组）的脑海马组织线粒体钙（ＭＣａ）、钙调素（ＣａＭ）、丙二醛（ＭＤＡ）及海马ＣＡ１ 区病理改变。结果　ＮＳ组海马组织ＭＣａ、ＣａＭ、ＭＤＡ含量显著升高（Ｐ＜ ０．０１）,海马ＣＡ１ 区神经元呈较严重缺血损伤性改变,而ＧＭ１ 组较ＮＳ组生化和病理变化明显改善。结论　ＧＭ１ 能改善脑缺血再灌注中钙平衡紊乱和氧自由基代谢异常,减轻脑缺血再灌注病理损伤。     

不同抗抑郁药物对抑郁症患者的疗效及对糖脂类代谢的影响

目的探讨不同抗抑郁药物对抑郁症患者的疗效及其对糖脂类代谢的影响。方法将我院收治的240例抑郁症患者随机分为三组,分别采用舍曲林、西酞普兰、米氮平治疗,分别为77例、80例、83例。比较三组患者治疗前后汉密尔顿抑郁量表(HAMD)评分、血糖水平及血脂水平的差异。结果治疗4周后、治疗8周后三组患者HAMD评分较治疗前显著下降(P0.05),米氮平组患者HAMD评分低于同期西酞普兰组、舍曲林组(P0.05);治疗4周后、治疗8周后西酞普兰组和舍曲林组患者HAMD评分,组间比较无明显差异(P0.05);治疗4周后、治疗8周后米氮平组、西酞普兰组患者空腹血糖(FPG)、餐后2h血糖(2h PG)、胆固醇(TC)、甘油三酯(TG)水平显著升高,也高于同期舍曲林组(P0.05);治疗4周后、治疗8周后米氮平组、西酞普兰组患者间2hPG、FPG、TC、TG水平无明显差异(P0.05);治疗4周后、治疗8周后舍曲林组患者2hPG、FPG、TC、TG水平较治疗前无明显差异(P0.05)。结论舍曲林、西酞普兰、米氮平对抑郁症患者临床效果佳;米氮平、西酞普兰较舍曲林对抑郁症糖脂代谢影响较大;舍曲林对抑郁症糖脂代谢影响较小,值得临床选择。     

不同糖浓度培养雪旺细胞对NGF及CGT基因表达的影响

目的通过观察不同糖浓度培养雪旺细胞NGF及CGT基因表达变化,探讨不同血糖浓度对周围神经的影响。方法首先将所培养的雪旺细胞分成正常对照组、低糖组、高糖组,采用RT-PCR技术,分别于培养后24 h、48 h、72 h对各组的NGF及CGT基因表达进行测定。结果NGF基因表达于高糖及低糖培养是下调,低糖更明显。CGT基因表达于高糖及低糖培养是上调,高糖及低糖表达无显著差异。结论本研究通过对NGF及CGT基因表达进行测定提示高糖、低糖对周围神经均有损伤,低糖表现更为明显。     

促红细胞生成素对血管性痴呆大鼠行为学及脑组织形态学的影响

目的永久性结扎双侧颈总动脉（2-VO）建立血管性痴呆（VaD）动物模型,观察EPO治疗对VaD大鼠行为学及脑组织形态学的影响。方法选用14～15月龄Wistar大鼠,应用水迷宫进行空间定向学习训练,将达到学会标准者随机分为3组：假手术（Sham）组、VaD组、VaD＋EPO腹部皮下注射治疗（EPO）组。2-VO制作VaD模型,应用水迷宫检测空间定向学习能力;行HE染色,透射电镜观察海马组织病理学变化。结果与Sham组比较,VaD组、EPO组2-VO后8周学习记忆能力均明显下降;VaD组2-VO术后8周海马CA1区锥体神经元细胞稀疏、肿胀,与VaD组相比,EPO组脑组织损伤程度明显减轻,学习记忆能力增强。结论2-VO可引起大鼠学习记忆能力下降,EPO治疗的VaD大鼠学习记忆能力明显增强;海马CA1区神经元的缺血损伤减轻可能是EPO改善VaD大鼠认知功能障碍的组织病理学基础。     

谷氨酸,γ—氨基丁酸对大鼠前包氏复合体神经元自发放电的影响

用多管微电极技术，在麻醉、自主呼吸的成年大鼠观察了微电泳谷氨酸（L-GLu）、γ-氨基丁酸（GABA）及其拮抗剂DL－2－氨基－5－磷酸戊酸（AP-5）、荷包牡丹碱（BIC）对前包氏复合体（pre－Botzingercomplex，preBotc）区神经元自发放电的影响，并测试了AP-5、BIC分别对L－Glu、GABA效应的阻断作用。结果显示，大多数被测试神经元（37／41个）被L－Glu兴奋，少数（4／41个）无反应：GABA使大多数被测试神经元（34／40个）抑制，对少数神经元（6／40个）无影响。AP-5对神经元放电无影响（19／34个）或产生抑制作用（15／34个）。BIC使神经元兴奋（10／30个）或无反应（20／30个）。L－Glu的兴奋作用和GABA的抑制作用呈量效依赖关系。9／21个受试神经元对L-Glu的兴奋反应被AP-5部分或完全阻断，大多数受试神经元（20／25个）对GABA的抑制反应被BIC部分或完全阻断。上述结果提示，成年大鼠pre－Botc区可能存在着内源性的Glu和GABA，它们分别通过NMDA受体和GABAA受体参与该区的神经信息传递过程。     

海藻酸钠-多聚赖氨酸-海藻酸钠微囊化大鼠卵巢激素分泌细胞异体移植对垂体形态学的影响

目的：已有研究证实海藻酸钠-多聚赖氨酸-海藻酸钠微囊对机体无明显毒副作用且生物相容性好，应用这一技术包裹细胞，可明显延长异体内移植物的存活时间。将海藻酸钠-多聚赖氨酸-海藻酸钠微囊化大鼠卵巢细胞体外培养后进行异体移植，观察其治疗卵巢功能丧失模型大鼠的可行性及垂体形态学变化。 方法：实验于2006-03/2007-09在首都医科大学生殖医学研究中心完成。①实验动物：30只Wistar雌性大鼠,随机分为正常对照组，卵巢摘除组，微囊移植组，每组10只。实验过程中对动物处置符合动物伦理学要求。②实验方法：卵巢摘除组：无菌条件下切除双侧卵巢；微囊移植组：海藻酸钠-多聚赖氨酸-海藻酸钠生物膜包裹传至P2代的大鼠卵巢细胞，制成微囊体外培养，收集24 h培养液以检测雌二醇分泌状态；将微囊化的卵巢细胞移植入已行双侧卵巢切除术的大鼠腹腔。用阴道涂片观察大鼠动情周期恢复情况。术后40 d麻醉后处死动物，放射免疫法检测血清雌二醇质量浓度，垂体组织常规石蜡包埋，连续切片，分别进行苏木精-伊红染色和雌、孕激素受体免疫组织化学染色。LEICA Q500IW自动图像分析仪对垂体细胞的面积，雌、孕激素受体吸光度值进行定量测定。 结果：①放射免疫法检测培养液显示，微囊化的卵巢激素分泌细胞具有继续合成和分泌雌二醇的功能。②检测血清中雌二醇质量浓度结果显示，卵巢摘除组明显低于正常对照组和微囊移植组，差异具有显著性意义，正常对照组和微囊移植组之间差异无显著性。③动情周期未恢复。④苏木精－伊红染色可见卵巢摘除组大鼠垂体中有大量阉割细胞,平均面积>180 μm2,与卵巢摘除组比较，微囊移植组大鼠垂体中细胞平均面积和阉割细胞数目均显著减少。⑤垂体雌、孕激素受体免疫组织化学吸光度值结果显示，卵巢摘除组明显低于正常对照组和微囊移植组，差异具有显著性意义。 结论：微囊化大鼠卵巢细胞异体移植后，可在受体大鼠体内继续合成和分泌雌二醇，并可以减少垂体内阉割细胞的形态和数目，提高垂体细胞雌激素受体和孕激素受体的表达，提示移植后细胞对垂体有反馈调节作用。     

姜黄素对AMPA/KA受体介导大鼠海马神经元钙内流的影响

目的 探讨姜黄素对α-氨基-3-羧基-5-甲基异恶唑-4-丙酸(AMPA)/海人酸(KA)受体介导大鼠海马神经元钙内流的影响.方法 选用胚胎17dSD鼠分离海马,离体培养海马神经元,借助活体钙荧光染色和激光共聚焦钙成像技术观察100μmol/LKA刺激海马神经元内钙的变化,不同浓度(5、10、15、30、50 μmol/L)姜黄素预孵育海马神经元30min对100μmol/L KA刺激下细胞内钙变化的影响,15 μmol/L姜黄素对不同浓度(10、30、50、100、200、300 μmol/L)KA刺激海马神经元内钙变化的影响.应用钴染色技术观察(30、100 μmol/L KA)刺激后海马神经元钴阳性染色细胞变化.姜黄素预孵育30min对KA刺激导致钴阳性染色细胞变化的影响.结果 不同浓度姜黄素预孵育30 min均可以明显缓解100 μmol/L或30 μmol/L KA导致的细胞内钙升高程度.差异均有统计学意义(P<0.05),其中15 μmol/L姜黄素作用最为明显.30μmol/L或100 μmol/LKA刺激均可以引起海马神经元钴染色阳性细胞增加,15 μmol/L姜黄素预处理30 min后明显减少钴染色阳性细胞,差异有统计学意义(P<0.05),而其他浓度(5 μmol/L或30 μmol/L)姜黄素未见明显影响.结论 一定浓度的姜黄素可以影响AMPA/KA受体介导大鼠海马神经元钙内流.这可能是姜黄素抗癫痫作用的一个机制.     

Pretreatment with SR48692 has different effects on central neurotensin-induced gastric mucosal defense and inhibition of gastric acid secretion in rats

Neurotensin is a tridecapeptide present in the brain and gastrointestinal tract. Administration of neurotensin into the brain results in responses in the gastrointestinal tract, suggesting a role for neurotensin in the interrelationships that comprise the brain–gut axis. Intracerebroventricular (i.c.v.) administration of neurotensin protects the gastric mucosa against injury caused by cold water restraint (CWR) and also inhibits gastrin-stimulated gastric acid secretion. The hypothesis tested was that these two actions of neurotensin are mediated via its high-affinity receptor. Rats were given neurotensin (60 μg, i.c.v.) prior to CWR or pylorus ligation after pretreatment with SR48692, a nonpeptide antagonist of the high-affinity neurotensin receptor (0.25 or 2.5 μg, i.c.v., or 10, 100, or 500 μg kg⁻¹, i.p.). Neurotensin reduced cold water restraint (CWR)-induced gastric mucosal injury and inhibited gastrin-stimulated acid secretion. Pretreatment with SR48692 (2.5 μg, i.c.v., or 100 μg kg⁻¹, i.p.) prior to CWR blocked neurotensin's protection of the gastric mucosa against injury. In contrast, pretreatment with 2.5 μg SR48692, i.c.v., did not block neurotensin-induced inhibition of acid secretion, whereas 500 μg kg⁻¹, i.p., partially blocked the inhibition. SR48692 (2.5 μg, i.c.v.) inhibited acid secretion, suggesting that SR48692 has agonist activity in this system. These results suggest that central neurotensin protects the gastric mucosa against CWR-induced injury via its high-affinity receptor. The receptor that mediates central neurotensin-induced inhibition of gastric acid secretion does not appear to be the high-affinity receptor since the neurotensin receptor antagonist SR48692, when given i.c.v., had agonist activity, inhibiting stimulated acid secretion. High-affinity neurotensin receptors in the periphery appear to play a role in inhibition of stimulated gastric acid secretion.     

Effect of naloxone on vagally-induced gastric acid secretion in rats

Previous studies in man and dogs have demonstrated that endogenous opioids participate in the stimulation of cephalic phase gastric acid secretion during indirect activation of the vagus. Since the effect of naloxone during direct vagal activation is unknown gastric acid secretion was assessed during electrical stimulation of the distal cut ends of both vagal nerves. In overnight fasted anesthetized rats the distal ends of the bisectioned cervical vagi were stimulated with 10V, 5Hz, 5 msec for 15 min. Vagal stimulation elicited an increase of gastric acid secretion by 5.6 mumol/min. Naloxone (1 mumol/kg.h) augmented gastric acid secretion significantly. Since this effect of naloxone was in contrast to previous data possible mechanisms of action of naloxone were examined that might help to explain this apparently inhibitory action of endogenous opioids on vagally-induced gastric acid secretion. The additional infusion of atropine or hexamethonium abolished the stimulatory effect of naloxone on vagally-induced acid secretion completely indicating that the action of naloxone depends on cholinergic background activity. Combined blockade of alpha- and beta-adrenergic receptors with phetolamine and propanolol reduced vagally-induced acid secretion in controls and during naloxone to a similar degree. Both adrenergic blocking agents also reduced the residual acid secretion observed during atropine or atropine + naloxone infusion. Measurements of plasma gastrin levels suggested that the naloxone-induced changes of acid secretion were not due to alterations of gastrin secretion. In summary these data demonstrate that vagally-induced acid secretion in anesthetized rats is largely due to cholinergic mechanisms with a small but separate contribution of adrenergic mechanisms. Endogenous opioids are activated during peripheral vagal stimulation attenuating vagally-induced acid secretion by modulation of cholinergic but not adrenergic mechanisms.     

Effect of food deprivation on mucus secretion of gustatory papilla in frogs

The innervation of taste buds, both in well-fed and starved frogs and its relation to mucopolysaccharide secretion has been investigated. In well-fed frogs the taste buds receive numerous intact nerve fibers, whereas in starved frogs the nerve fibers are present, but in various stages of degeneration. There is a significant reduction in the width of taste buds, the height of nonciliated cylinder cells, and the height of basal cells of taste buds in starved frogs compared to the taste buds of well-fed frogs. It is suggested that the nervous influence plays an important role in nonciliated cylinder cells which secrete acid mucopolysaccharide.     

Effect of different frequencies of repetitive transcranial magnetic stimulation on acquisition of chemical kindled seizures in rats

In the current study we investigated the effect of repetitive transcranial magnetic stimulation (rTMS) at different frequencies on chemical kindling in rats. Chemical kindling was induced by injection of pentylenetetrazol (PTZ; 45 mg/kg) at the intervals of 48 h between the injections. In the first experiment, effect of 0.25, 1 and 5 Hz rTMS (four trains of 4 s at motor threshold intensity) on kindling acquisition was investigated. In the second experiment, the stability of rTMS effects was checked in animals of the first experiment during a follow-up period of 2 weeks. Animals received a single dose of PTZ at 7th and 14th day after the last PTZ injection (12th injection) and their seizure parameters were recorded. Obtained results showed that application of rTMS at the frequencies of 0.25 and 1 Hz had anticonvulsant effect and decreased the PTZ kindling acquisition. However, when applied at the frequency of 5 Hz, it had an increasing effect on PTZ kindling rate. During the follow-up study, the seizure severity increased in animals treated with 0.25 Hz rTMS (and somehow in animals treated with 1 Hz rTMS), but did not change in animals treated with 5 Hz rTMS compared to the 12th PTZ injection. Our results showed that rTMS application may have an anticonvulsant effect during chemical kindling acquisition at very low frequency (0.25 Hz) and can increase the seizure severity at high frequency (5 Hz). However, during follow-up, the anticonvulsant effects of rTMS may be converted to proconvulsive effects.     

Intrahypothalamic microinfusion of corticotropin-releasing factor inhibits gastric acid secretion but increases secretion volume in rats

Bilateral microinfusion of synthetic ovine corticotropin releasing factor (oCRF; 0-4.0 microgram/rat [0-856 pmol/rat]) into the paraventricular nucleus or the ventromedial nucleus of the rat hypothalamus inhibited gastric acid secretion in a dose-related manner. Unexpectedly, these microinfusions both decreased acid concentration and increased secretion volume; total acid output (acid concentration multiplied by secretion volume) was strongly inhibited. In the lateral hypothalamus. CRF microinfusion also both decreased acid concentration and increased secretion volume, but total acid output did not change. oCRF microinfusion into the caudate-putamen did not significantly affect any measure of gastric acid secretion even at the highest dose used. The increased secretion volume seen after oCRF microinfusion is unique; all other centrally acting inhibitors of gastric acid secretion decrease secretion volume. It is possible that hypothalamic CRF may influence gastric secretory function.     

Stimulatory effects of centrally injected kainate and N-methyl-D-aspartate on gastric acid secretion in anesthetized rats

The effects of N-methyl-D-aspartate (NMDA), kainate and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), ionotropic glutamate agonists, on gastric acid secretion were investigated in the continuously perfused stomach of anesthetized rats. The lateral ventricular (LV) injection of kainate (0.01-1 microg) or NMDA (0.3-3 microg) dose-dependently stimulated gastric acid secretion. AMPA (3-10 microg) also stimulated gastric acid secretion but the effect was very weak. Repeated injections of kainate (0.1 microg) or NMDA (1 microg), at least twice, stimulated gastric acid secretion to a similar degree. The effect of kainate (0.1 microg) was blocked by the kainate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione disodium (3 microg, LV) and D-gamma-glutamylaminomethanesulfonic acid (30 microg, LV), but not by NMDA receptor antagonists. The effect of NMDA (10 microg) was blocked by (+/-)-3-(2-carboxypiperazin-4-yl)-1-propylphosphonic acid (10 microg, LV), a competitive NMDA receptor antagonist, and (+)-5-methyl-10,11-dihydro-5H-dibenzocyclo-hepten-5,10-imine hydrogen maleate (10 microg, LV), a non-competitive NMDA receptor antagonist, but not by kainate receptor antagonists. Moreover, the gastric acid secretion stimulated by kainate and NMDA were completely blocked by systemic atropine injection (1 mg/kg, i.v.) and vagotomy. These findings suggest that kainate and NMDA receptor mechanisms are independently involved in the central nervous system to control gastric acid secretion through vagus cholinergic activation.     

复合振动对卵巢切除大鼠骨质量的作用

背景：目前所使用的全身振动防治骨质疏松所需振动强度较大,人体不适感较强。作者设计了复合振动,前期实验发现复合振动可在更低强度下有效预防卵巢切除大鼠的骨密度下降。 目的：课题创新性提出低强度复合振动可维持生长期卵巢切除SD大鼠骨质量的理论假设,并期望实验结果加以验证。 方法：SPF级4月龄雌性未育SD大鼠32只,随机分为正常对照组、卵巢切除组以及振动1、振动2组,每组大鼠均为8只。振动1组接振45~55 Hz,0.05~0.1 g;振动2组接振45~55 Hz,0.12~0.21 g。振动20 min/次,1次/d,5次/周,休息间隔不大于2 d。实验时间13周。观察振动干预前后大鼠活体骨密度,体外标本骨微结构以及生物力学性能。 结果与结论：卵巢切除组腰椎骨密度下降(P < 0.05),而正常对照组与两振动组有显著性增加,股骨骨密度均增加,组间差异无显著性意义;卵巢切除各组骨微结构参数均明显下降,但振动2组骨小梁数量、骨小梁厚度、骨小梁间距、骨体积分数相对于卵巢切除组有显著改善;腰椎骨强度值两振动组较卵巢切除组显著增加(P=0.025、0.006),与正常对照组比较差异无显著性意义。实验结果证明,特定的复合振动舒适感较好的低强度下可以有效预防卵巢切除SD大鼠骨密度下降,减轻骨微结构破坏程度,维持骨强度,具有改善卵巢切除大鼠骨质量的作用和潜在的预防骨质疏松作用。     

Effect of selective gastric vagotomy on gustatory behavior in rats

Gustatory responses were investigated in sham vagotomized (SVgX) and selective gastric vagotomized (VgX) male rats by 1-h single-bottle tests using 3% sucrose, 13% glucose, 0.2% saccharin, 0.9% sodium chloride, 0.16% citric acid, 0.001% quinine sulphate and tap water as test solutions. The intakes of sucrose, glucose, saccharin and sodium chloride were significantly less in VgX rats, compared to SVgX ones. When all these rats were exposed to graded concentrations of sucrose (0.1%, 0.5%, 1% and 5%), a maximum preference was shown to 5% and the least to 0.1% sucrose by both SVgX and VgX rats, even though the VgX rats consumed less than SVgX ones. Vagotomy produced a maximum suppression of 5% sucrose intake, a moderate suppression of 1% and 0.5% sucrose intake and no significant change in the intake of 0.1% sucrose. The results also indicated a probable reduction in the ability of VgX rats to discriminate taste intensities within a close range. Pharmacological blocking of vagal efferents with atropine methyl nitrate (5 mg/kg) did not produce any significant change in the intakes. The possibility of an excitatory input through the gastric vagal afferents selectively influencing the intake of sapid substances is suggested.